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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Left-sided congestive heart failure may be secondary to decreased left ventricular myocardial compliance in some patients. To investigate the anatomic basis for altered wall stiffness, morphometric determinations of muscle cell nuclear density and percent of myocardium consisting of muscle cells were made for right and left ventricular free wall and septum in 127 hearts with normal coronary arteries. The hearts were normal (33 patients), had left ventricular hypertrophy (28 patients), right ventricular hypertrophy (25 patients), or chronic dilatation (41 patients). With cardiac enlargement, the average percent of myocardium consisting of muscle did not change from the approximately 75% value characteristic of normal hearts. In contrast, muscle cell nuclear density decreased proportionate to cardiac enlargement, demonstrating that muscle cell hypertrophy, not hyperplasia, is the basis for weight increase. Some hearts with marked longstanding dilatation also had perivascular and interstitital "striae" of connective tissue differing from replacement fibrosis. An increase in epicardial coronary artery caliber commensurate with increased heart weight suggests that ischemia is not the basis of connective tissue increase. The results show that cardiac muscle cell hypertrophy is accompanied by commensurate increase in interstitial connective tissues. This pattern of myocardial growth with cardiac enlargement may produce increased myocardial stiffness simply as a result of increased wall thickness, and may lead to left-sided congestive heart failure.
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PMID:Constituents of the human ventricular myocardium: connective tissue hyperplasia accompanying muscular hypertrophy. 644 58

Changes in dietary lipid intake are known to alter the fatty acid composition of cardiac muscle of various animals. Because changes in cardiac muscle membrane structure and function may be involved in the pathogenesis of arrhythmia and ischemia, we have examined the effects of dietary lipid supplements on the phospholipid distribution and fatty acid composition of rat atria and ventricle following 20 weeks feeding of diets supplemented with either 12% sunflower-seed oil or sheep fat. Neither lipid supplement produced significant changes in the proportions of cholesterol, total phospholipids or phosphatidylcholine, phosphatidylethanolamine or diphosphatidylglycerol,--the phospholipid classes that together account for more than 90% of the total phospholipids of rat cardiac muscle. Significant changes were found in the profiles of the unsaturated fatty acids of all 3 phospholipid components of both atria and ventricle. Although similar, the changes between these tissues were not identical. However, in general, feeding a linoleic acid-rich sunflower seed oil supplement resulted in an increase in the omega-6 family of fatty acids, whereas feeding the relatively linoleic acid-poor sheep fat supplement decreased the level of omega-6 fatty acids but increased the levels of the omega-3 family, resulting in major shifts in the proportions of these families of acids. In particular, the ratio of arachidonic acid: docosahexaenoic acid (20:4,omega-6/22:6,omega-3), which is higher in all phospholipids of atria than ventricle, is increased by feeding linoleic acid, primarily by increasing the level of arachidonic acid in the muscle membranes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The composition of cardiac phospholipids in rats fed different lipid supplements. 671 52

In this study we have compared myocardial lesions induced by catecholamines and coronary occlusion and reperfusion injuries in rats. Although microcirculatory factors were found to play an important role in catecholamine-induced cardiac muscle cell injury, alterations in sarcolemmal membrane permeability suggest a direct cardiotoxic effect. Cardiac muscle cells damaged irreversibly by ischemia reveal sarcomeres in extreme relaxation and mitochondria with floccular densities; cardiac muscle cells that die following reperfusion exhibit contraction band formation and mitochondria with calcium phosphate deposits. The ultrastructural appearance of reperfused ischemic cardiac muscle cells was similar to that observed following administration of catecholamines. These morphological similarities suggest a common causal pathway for stress-induced and ischemic heart diseases.
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PMID:Reperfusion injury. A possible link between catecholamine-induced and ischemic myocardial alterations. 685 68

FFA are the main substrate of biological oxidation in cardiac muscle under normal conditions. But it could be shown in man and animal that during heavy exercise there is a shift to preferential oxidation of lactate. During oxygen deficiency in hypoxic or ischemic situations which may occur lightly in distinct areas of hypertrophic hearts after exercise, lactate, alpha-glycerol phosphate and acyl-CoA as well as triglyceride levels in cardiac tissue may increase, whereas FFA are less oxidized. Unoxidized intracellular FFA and acyl-CoA, which are not esterified in a sufficient way to triglycerides, may impair oxidative phosphorylation in mitochondria, the P/O quotient as well as cardiac function perhaps by an interference with Ca++ movements during the contraction cycle. With the examples of anoxia and complete ischemia as the two extreme situations of O2 deficiency some principles of the alteration of cardiac metabolism are pointed out, and furthermore attempts to improve anoxic tolerance of cardiac tissue.
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PMID:Some aspects on the regulation of carbohydrate and lipid metabolism in cardiac tissue. 699 68

An electron microscopic investigation on reparative regeneration of the myocardium has been performed in dogs survived after clinical death resulted from loss of blood. Some regenerative processes already begin on the first hours after reanimation and they proceed on the background of certain distrophic and destructive changes. On the 3d-7th days of the restorative period, the intracellular regeneration of cardiomyocytes increases considerably; it is demonstrated by newly formed myofilaments in the foci of myofibrillar lysis, increasing content of small mitochondria, hyperplasia of the granular endoplasmic reticulum. Simultaneously, a great number of secondary lysosomes is forming; as a result, the cells are releasing themselves from the substances formed after decomposition and decay of some organelles. Myelin-like bodies are observed to be pushed out of the cardiomyocytes into the intercellular space. In fact, by the end of the second week after total ischemia the structure of the cardiac muscle is fully normalized. T-system of cardiomyocytes is the one which is the slowest to restore.
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PMID:[Morphologic changes in the myocardium following acute blood loss and subsequent resuscitation]. 706 12

A new nonrotating multiple biopsy device has been developed to allow the rapid, simultaneous and contiguous sampling of cardiac muscle in the large mammalian heart. Each cutter obtains 40 adjacent transmural left ventricular biopsy samples, each of 4 mm section. The epicardial 1.8 mm of each biopsy section was analyzed for flow, adenosine triphosphate, adenosine diphosphate, adenosine monophosphate, creatine phosphate and lactate. Use of this procedure in the dog heart 30 minutes after coronary arterial ligation permitted characterization of the nature of flow and metabolic gradients as the sampling site moved from the core of an areas of regional ischemia to the surrounding normal tissue. These studies of metabolic and flow geometry in the lateral plane indicate the existence of a sharp interface of flow and metabolism between normal and ischemic tissue. The absence of intermediate levels of flow and metabolism indicate that, in the lateral plane at least, a quantitatively significant and spatially identifiable "border zone" region does not exist. However, these findings, do not preclude the existence of such a zone of jeopardized tissue in the transmural plane or the occurrence of a temporal border zone to which interfaces of flow and metabolism may migrate with time.
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PMID:Characterization of the lateral interface between normal and ischemic tissue in the canine heart during evolving myocardial infarction. 723 97

During global ischemia in isolated rat hearts, the development of contracture, due to irreversible myofilament sliding, causes reduction of left ventricle luminal volume. Also, a considerable area of the myocardium cannot be reperfused after 1 hour's global ischemia. The purpose of this study was to reduce myofilament sliding by placing a fluid-filled isovolumic balloon in the left ventricular cavity of isolated rat hearts and assess the extent of reflow, after 60 minutes' ischemia, by perfusion of a 1% fluorescein tracer solution. Light and electron microscopy was used to determine the state of the vasculature and myofibrillar apparatus. In hearts without the left ventricular balloon (control) the ischemia produced a no-reflow zone comprising 45% of the myocardial wall. In contrast, if an isovolumic balloon was in place during the ischemic period, only 6% of the wall was involved. The volume of the capillary bed in the subendocardium of the control hearts was about 60% of that in th isovolumic hearts. In the isovolumic ("isometric") mode, ischemic contracture was associated with more severe myocardial cell injury than in the corresponding control ("isotonic") mode. Our results support the concept that intramyocardial pressure generated by ischemic contracture plays a major role in the production of the no-reflow phenomenon in globally ischemic rat hearts, and indicate that it is the series elastic component of cardiac muscle which imparts the stiffness necessary to prevent reopening of coronary vessels after a severe ischemic insult.
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PMID:The effect of an isovolumic left ventricle on the coronary vascular competence during reflow after global ischemia in the rat heart. 726 Dec 72

In the cross-circulated canine heart-lung preparation, the stroke volume (SV) or the end-systolic volume increased linearly with increasing end-diastolic volume (EDV) when the afterloading impedance was fixed. Exactly the same result was obtained in the relation between the initial length (I) and the amount of shortening (S) for the tetanic contraction of isolated frog ventricular muscle. The slope of the EDV-SV or I-S relation was less than 1.0, suggesting that a kind of depressive effect or a deactivation of contraction was working during the active shortening of cardiac muscle. The slope, which inversely reflects the degree of deactivation, slightly tended to 1.0 with decreasing load and markedly by inotropic intervention, but it was not changed by partial ischemia. The horizontal axis intercept of the EDV-SV or I-S relation, which reflects the ability of the cardiac muscle to shorten under a specified afterloaded condition, shifted to the right (the ability decreased) at a larger load or under partial ischemia but shifted to the left with inotropic intervention. The deactivation increased linearly with the amount of active shortening but no deactivation was observed when there was no active shortening or no load. The mechanism of the deactivation is not due to a shortage of active-state duration but probably due to a depressive effect on Ca2+ utilization of the contractile system during the sliding phase of myofilaments.
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PMID:Depressive effects of active shortening on stroke volume of left ventricle and shortening amount of isolated ventricular muscle. 728 25

Fresh autologous thrombus, 1.0 to 1.5 ml, was injected into the left anterior descending and/or left diagonal coronary arteries of 19 open-chest dogs to produce evolving acute myocardial infarction (AMI). Thrombotic obstruction was documented by coronary angiography. Multilead epicardial ECGs showed ST segment elevations of affected left ventricular (LV) areas within 2 minutes after thrombus injection, and LV segmental wall cyanosis with hypocontraction was observed within 10 minutes in the myocardial areas supplied by the thrombosed artery. Ten animals then received an initial dose of streptokinase (STK), 250,000 U (intravenous), followed by STK, 1000 to 3000 U/min (intracoronary), while nine control dogs untreated with STK received normal saline infusion. All but one STK-treated animal (all nine animals receiving intracoronary STK) had reestablishment of blood flow in the previously occluded vessels within 1 1/2 hours, disappearance of ventricular cyanosis, return of normal LV contractile function, and normalization of elevated ST segments within 1 hour after intracoronary STK therapy. In contrast, in the non-STK-treated control group, all animals had continued coronary obstruction, progressive ST elevations, and worsening LV cyanosis and hypocontraction until death or for more than 3 hours post thrombus; three control animals died of ventricular fibrillation (VF) within 1 hour of thrombus occlusion, three more died of VF within 2 hours post thrombus, and only three survived beyond 2 hours post thrombus. Postmortem examination of non-STK-treated animals revealed extensive residual coronary thrombus. All intracoronary STK-treated animals evidenced absence of residual coronary thrombus at postmortem examination. These data provide clinically relevant evidence that early intracoronary STK effects thrombolysis in AMI by reopening coronary vessels occluded by fresh thrombus, thereby protecting myocardium from further ischemia and necrosis, preserving LV function, and also reversing cardiac muscle injury.
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PMID:Experimental reversal of acute coronary thrombotic occlusion and myocardial injury in animals utilizing streptokinase. 731 18

Ischemia of the rat brain led to permanent increase in oxygen consumption, sharp phasic changes of oxydative phosphorylation, and fall of the P/O coefficient in the brain mitochodria which indicates a dissociation between respiration and phosphorylation. During the postischemic period all the parameters become normal. Oxygen consumption in the cardiac mitochondria is only enhanced in the early (15 min of circulatory hypoxia--CH) and late (72 hrs of CH) periods of CH. The oxydative phosphorylation is particularly low at 15 min and at 24-hr duration of CH. During the posthypoxic period the oxygen consumption is significantly enhanced but it drops lower than control level after 24-hr CH. The changes of oxydative phosphorylation occur in phases. The P/O coefficient is minimal in the posthypoxic period after the 15-min CH. Disturbances of oxydative metabolism seem lesser in the cardiac mitochondria. The changes occurring in the cardiac muscle during cerebral CH seem to underlie different signs of the cerebro-cardiac syndrome in brain pathology.
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PMID:[Heart and brain tissue mitochondrial respiration and oxidative phosphorylation during cerebral circulatory hypoxia and in the posthypoxic period]. 739 34


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